It is well known that dental caries is an infectious disease which results in the progressive destruction of both inorganic and organic tooth substance. The caries process is initiated by the interplay of microorganisms adhering to tooth surfaces and a carbohydrate substrate in contact with a susceptible tooth surface. The caries lesion invariably originates on the external surface of the enamel of erupted teeth or on the exposed cementum of root surfaces and the process then progresses centripetally deep into the dentin.
The dental caries starts with the production of acids as a result of fermentation of the carbohydrate substrate by the microorganisms. These acids result in demineralization of localized tooth tissue. Consequently, the destruction of hard tissues, such as enamel, dentin, cementum or bone starts with the dissolution of the inorganic material of these tissues, namely hydroxyapatite.
In the case of mature enamel this also results in the decomposition of the organic matrix since this constitutes only 2% of the total composition of the enamel. The situation is different in other hard tissues (dentin, cementum and bone) which consists of highly cross-linked collagen matrix which is resistant to degradation under conditions capable of causing demineralization of these tissues (weak acids or calcium-chelating agents).
Native collagen is resistant to general proteolytic digestion under physiological conditions (e.g. by proteolytic enzymes such as trypsin and chemotrypsin) due to its triple polypeptide helix structure. However, collagen can be cleaved by tissue collagenases into two large fragments which can then be further cleaved by non-specific peptidases.
We have found in studies which we have made that dentin material derived either from carious teeth or from intact teeth (human) contains collagenolytic activity, the carious dentin being significantly more active. This fact would appear to indicate that during the tooth development there is produced, besides the collagen, also collagenase in an inactive form, which may become activated in the course of the carious process and is consequently capable of degrading the collagen matrix of the dentin. Thus, we have found that practically the entire collagenolytic activity in the process of the carious disease originates from the collagenase of the dentin itself, although it is known that some bacteria involved in the carious process are capable of secreting collagenase enzymes of their own.